Dysregulation of histone deacetylases in carcinogenesis and tumor progression: a possible link to apoptosis and autophagy

Patra, Srimanta; Panigrahi, Debasna Pritimanjari; Praharaj, Prakash Priyadarshi; Bhol, Chandra Sekhar; Mahapatra, Kewal Kumar; Mishra, Soumya Ranjan; Behera, Bishnu Prasad; Jena, Mrutyunjay; Bhutia, Sujit K.

doi:10.1007/s00018-019-03098-1

Cited by 31 publications

(15 citation statements)

References 131 publications

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“…Additionally to mitochondria and the immune system, community 36 has been associated to gender, in line with the higher risk of females to develop Alzheimer’s disease, in opposition to lung cancer, which is more frequent in men [44,45]. Histone deacetylase (HDAC), associated to community 22, confirms the known involvement of HDAC1 in both cancer and Alzheimer’s disease [46,47]. Community 30 is enriched in focal adhesion.…”

Section: Resultsmentioning

confidence: 92%

Molecular Inverse Comorbidity between Alzheimer’s Disease and Lung Cancer: New Insights from Matrix Factorization

Greco

Valle

Pancaldi

et al. 2019

IJMS

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Matrix factorization (MF) is an established paradigm for large-scale biological data analysis with tremendous potential in computational biology. Here, we challenge MF in depicting the molecular bases of epidemiologically described disease–disease (DD) relationships. As a use case, we focus on the inverse comorbidity association between Alzheimer’s disease (AD) and lung cancer (LC), described as a lower than expected probability of developing LC in AD patients. To this day, the molecular mechanisms underlying DD relationships remain poorly explained and their better characterization might offer unprecedented clinical opportunities. To this goal, we extend our previously designed MF-based framework for the molecular characterization of DD relationships. Considering AD–LC inverse comorbidity as a case study, we highlight multiple molecular mechanisms, among which we confirm the involvement of processes related to the immune system and mitochondrial metabolism. We then distinguish mechanisms specific to LC from those shared with other cancers through a pan-cancer analysis. Additionally, new candidate molecular players, such as estrogen receptor (ER), cadherin 1 (CDH1) and histone deacetylase (HDAC), are pinpointed as factors that might underlie the inverse relationship, opening the way to new investigations. Finally, some lung cancer subtype-specific factors are also detected, also suggesting the existence of heterogeneity across patients in the context of inverse comorbidity.

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Section: Resultsmentioning

confidence: 92%

Molecular Inverse Comorbidity between Alzheimer’s Disease and Lung Cancer: New Insights from Matrix Factorization

Greco

Valle

Pancaldi

et al. 2019

IJMS

View full text Add to dashboard Cite

show abstract

“…Additionally to mitochondria and immune system, community 36 has been associated to gender, in line with the higher risk of females to develop Alzheimer's disease, in opposition to lung cancer, which is more frequent in men [44,45]. Histone Deacetylase (HDAC), associated to community 22, confirms the known involvement of HDAC1 in both cancer and Alzheimer's disease [46,47]. Community 30 is enriched in focal adhesion.…”

Section: New Biological Insights On the Inverse Comorbidity Between Amentioning

confidence: 80%

Molecular Inverse Comorbidity between Alzheimer’s disease and Lung Cancer: new insights from Matrix Factorization

Greco

Valle

Pancaldi

et al. 2019

Preprint

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Matrix Factorization (MF) is an established paradigm for large-scale biological data analysis with tremendous potential in computational biology.We here challenge MF in depicting the molecular bases of epidemiologically described Disease-Disease (DD) relationships. As use case, we focus on the inverse comorbidity association between Alzheimer's disease (AD) and lung cancer (LC), described as a lower than expected probability of developing LC in AD patients. To the day, the molecular mechanisms underlying DD relationships remain poorly explained and their better characterization might offer unprecedented clinical opportunities.To this goal, we extend our previously designed MF-based framework for the molecular characterization of DD relationships. Considering AD-LC inverse comorbidity as a case study, we highlight multiple molecular mechanisms, among which the previously identified immune system and mitochondrial metabolism. We then discriminate mechanisms specific to LC from those shared with other cancers through a pancancer analysis. Additionally, new candidate molecular players, such as Estrogen Receptor (ER), CDH1 and HDAC, are pinpointed as factors that might underlie the inverse relationship, opening the way to new investigations. Finally, some lung cancer subtype-specific factors are also detected, suggesting the existence of heterogeneity across patients also in the context of inverse comorbidity.

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“…The histone modification patterns are crucial for the organization and maintenance of chromatin and as a result, transcriptional regulation. These processes are fundamental in understanding epigenetic mechanisms and their involvement in cancer development, as transcriptional control is essential for appropriate cell proliferation and differentiation[98,99].…”

Section: Habp4 and Serbp1 Involvement In Cancermentioning

confidence: 99%

Complex interactomes and post-translational modifications of the regulatory proteins HABP4 and SERBP1 suggest pleiotropic cellular functions

Colleti

Melo‐Hanchuk

Silva

et al. 2019

WJBC

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The 57 kDa antigen recognized by the Ki-1 antibody, is also known as intracellular hyaluronic acid binding protein 4 and shares 40.7% identity and 67.4% similarity with serpin mRNA binding protein 1, which is also named CGI-55, or plasminogen activator inhibitor type-1-RNA binding protein-1, indicating that they might be paralog proteins, possibly with similar or redundant functions in human cells. Through the identification of their protein interactomes, both regulatory proteins have been functionally implicated in transcriptional regulation, mRNA metabolism, specifically RNA splicing, the regulation of mRNA stability, especially, in the context of the progesterone hormone response, and the DNA damage response. Both proteins also show a complex pattern of post-translational modifications, involving Ser/Thr phosphorylation, mainly through protein kinase C, arginine methylation and SUMOylation, suggesting that their functions and locations are highly regulated. Furthermore, they show a highly dynamic cellular localization pattern with localizations in both the cytoplasm and nucleus as well as punctuated localizations in both granular cytoplasmic protein bodies, upon stress, and nuclear splicing speckles. Several reports in the literature show altered expressions of both regulatory proteins in a series of cancers as well as mutations in their genes that may contribute to tumorigenesis. This review highlights important aspects of the structure, interactome, post-translational modifications, sub-cellular localization and function of both regulatory proteins and further discusses their possible functions and their potential as tumor markers in different cancer settings.

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Dysregulation of histone deacetylases in carcinogenesis and tumor progression: a possible link to apoptosis and autophagy

Cited by 31 publications

References 131 publications

Molecular Inverse Comorbidity between Alzheimer’s Disease and Lung Cancer: New Insights from Matrix Factorization

Molecular Inverse Comorbidity between Alzheimer’s Disease and Lung Cancer: New Insights from Matrix Factorization

Molecular Inverse Comorbidity between Alzheimer’s disease and Lung Cancer: new insights from Matrix Factorization

Complex interactomes and post-translational modifications of the regulatory proteins HABP4 and SERBP1 suggest pleiotropic cellular functions

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